Evidence map›Paper›PMID 41402588›Full record

ArticleScientific reports2025

Cedrol mitigates hepatic lipid accumulation and adipocyte hypertrophy induced by corticosteroids through the inhibition of glucocorticoid receptor activity.

Minghui Shu, Pan Wang

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Minghui ShuShenzhen Key Laboratory of Steroid Drug Discovery and Development, School of Medicine, The Chinese University of Hong Kong, Shenzhen, 518172, Guangdong, China.
Pan WangShenzhen Key Laboratory of Steroid Drug Discovery and Development, School of Medicine, The Chinese University of Hong Kong, Shenzhen, 518172, Guangdong, China. wangpan@cuhk.edu.cn.ORCID http://orcid.org/0000-0002-0719-1175

Funding

Ganghong Young Scholars Development Fund 1011E0009, 1011E0031Shenzhen-Hong Kong Cooperation Zone for Technology and Innovation HZQB-KCZYB-1010056Shenzhen Key Laboratory of Steroid Drug Discovery and Development ZDSYS10190901093417963Shenzhen Science and Technology Program JCYJ20220818103008017
6 · The paper itself

Abstract

Cedrol is a sesquiterpene alcohol derived from ginger and cedar oil. Cedrol has multiple pharmacological effects such as sedation, promoting hair growth, decreasing blood pressure and reducing obesity. But its pharmacological mechanisms are not fully understood and its direct targets remain unknown. Glucocorticoids, particularly dexamethasone, are stress hormones in the body and interact with glucocorticoid receptors (GRs) to regulate physiological functions such as metabolism. In this study, we find that cedrol effectively mitigates the lipid accumulation in liver and adipose tissues induced by dexamethasone in adult male mice. Cedrol treatment also inhibits the dexamethasone-induced expression of genes involved in lipid metabolism, including Cd36, C/ebpβ, Srebp1, Fas and Scd1 in the liver. In addition, cedrol binds to GR in the cellular thermal shift assay and shows antagonistic activity in luciferase reporter assays. These results indicate that cedrol has GR antagonist activity, which may be responsible for its effect on lipid metabolism, and suggest that cedrol could also be potentially used in the treatment of lipid metabolism disorders induced by high glucocorticoids.

Indexed as

AdipocytesLipid MetabolismLiverReceptors, GlucocorticoidAnimalsDexamethasoneGlucocorticoidsMaleMiceMice, Inbred C57BLDexamethasoneGlucocorticoidsReceptors, GlucocorticoidAntagonismCedrolGlucocorticoid receptorLipid metabolism

Identifiers

PMID41402588
PMCPMC12830865

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.